In this paper, Michael Duchêne and colleagues have sought systematically for novel target proteins of thioredoxin in Entamoeba histolytica, the causative agent of amoebiasis, in order to extend our knowledge of its physiological significance in the parasitic cell and to identify the cellular pathways that could be indirectly affected by metronidazole treatment.

In this paper, Mario Barros and colleagues show how the impairment in the oxidation of cytosolic NADH by Nde1p, one of three distinct inner mitochondrial membrane NADH dehydrogenases in Saccharomyces cerevisiae, is deleterious towards mitochondrial biogenesis due to an increase in reactive oxygen species release.

In this paper, Clare Hawkins and colleagues have characterized the structural and functional modifications of lipid-free apoA-I (apolipoprotein A1) and rHDL (reconstituted discoidal high-density lipoprotein) containing apoA-I complexed with phospholipid, induced by HOSCN (hypothiocyanous acid) and its decomposition product, OCN^- (cyanate), and show how the ability of HOSCN to impair apoA-I-mediated cholesterol efflux may contribute to the development of atherosclerosis, especially in smokers who have high plasma levels of SCN- (thiocyanate).

In this paper, Kenneth Humphries and colleagues have evaluated cardiac mitochondrial function in a rodent model of chronic Type 1 diabetes before the onset of contractility deficits, and show that the most pronounced change is severe metabolic inflexibility, with hyperacetylation of protein lysine also observed.